The morbidly obese human has an increased incidence of diabetes, hypertension, hyperlipidemia, respiratory failure, and venous insufficiency of the lower extremities. These conditions may shorten the life expectancy of these individuals as well as impair their social and physical well being. Surgical bypass of large amounts of the small intestine has been demonstrated to force weight loss and to alter favorably the diabetic, hypertensive, and hyperlipidemic states of these patients. While small intestinal bypass for obesity produces a number of pathologic conditions, including malabsorption, rheumatism, and renal oxalate stone formation, the occurrence of increased hepatic lipid accumulation with subsequent liver failure and cirrhosis produces significant mortality limiting the applicability of the operation. The proposed research utilizes a rat model to evaluate hepatic lipid metabolism following small intestinal bypass. The suitability of the rat as an animal model is related to the hyperphagia of this animal under certain dietary conditions resulting in nutritional obesity, the presence of congenitally obese rat models, and to the ready tolerance of the rat for bypassing 90 percent of the small intestine. The proposed research has demonstrated that a non-obese rat does not accumulate lipid in the liver following bypass of 78 percent of the small intestine suggesting that nutritional or hereditary depots of excess fat are required to produce hepatic steatosis in rats. Subsequent studies demonstrated that mobilization of large amounts of fat in humans following small intestinal bypass does not inherently produce pathologic accumulations of fat in the liver. Continued evaluation of hepatic lipid metabolism in an animal model may delineate a specific defect in lipid metabolism associated with small intestinal bypass which may be correctable and directly applicable to the problem in humans. BIBLIOGRAPHIC REFERENCE: Kaminski DL, Jellinek M. Ruwart M, Mueller EJ and Menz L: Small intestinal bypass in nutritionally obese rats receiving choline supplement. Surg Forum 27:449-451, 1976.